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We are plant extract suppliers supplier. Among them, flavones isolated from Scutellaria baicalensis root exhibit strong neuroprotective effects on the brain and are not toxic in the broad range of tested doses. Their neuroprotective potential has been shown in both oxidative stress-induced and amyloid-beta and alpha-synuclein-induced neuronal death models. In the preliminary study, wogonin, another flavone from Scutellaria baicalensis root, has been shown to stimulate brain tissue regeneration, inducing differentiation of neuronal precursor cells.

Scutellaria Baicalensis Georgi

Salicin is a naturally occurring compound found in the bark of several species of trees, primarily North American in origin, that are from the willow, poplar, and aspen families. We are Scutellaria Baicalensis Georgi. White willow, from whose Latin name, Salix alba, the term salicin is derived, is the most well known source of this compound, but it is found in a number of other trees, shrubs, and herbaceous plants as well being synthesized commercially. It is a member of the glucoside family of chemicals and is used as an analgesic and antipyretic.

Salicin Extract

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CHICAGO, May 4 — A February 1999 Joint Expert Committee on Food Additives (JECFA), report which has just become available, claims that the natural sex hormones, estradiol, progesterone and testosterone, can be safely used for growth promotion of cattle in feed lots without risks to consumers, particularly of breast and other reproductive cancers. The report established "Acceptable Daily Intakes" (ADI's) or safe threshold tolerances for these natural hormones on the basis of "hormone-dependent parameters," which were accepted as the determinants of carcinogenicity. This novel proposal is scientifically invalid. It is also in diametric opposition to 1997 World Trade Organization (WTO) testimony opposing the EU ban on hormonal meat by US and Canadian experts, some of whom also authored the 1999 report. — While the latest JECFA report admits that estradiol is a gene-damaging (genotoxic) carcinogen, it fails to recognize that this precludes the establishment of an ADI. Setting this ADI also contradicts illustrative WTO testimony by US/Canadian experts: "— chemicals which produce carcinogenicity through a clear genotoxic mechanism should be regulated as if a threshold dose cannot be derived and hence an — ADI - cannot be proposed"; and "— the ADI model does not predict quantitative risks and is not applicable to genotoxic carcinogens." Of related interest is recent confirmation by FDA scientists on the absence of a threshold for estradiol in experimental studies on estradiol-induced sex reversal.

The 1999 JECFA report emphasized that the carcinogenicity of estradiol is due to its hormonal effects "— which occur at much lower doses than other toxicological effects —," on whose basis ADIs were developed. However, the report ignores well documented and long-standing evidence that estradiol is carcinogenic in non-hormone dependent tissues including liver and skin (malignant melanoma) in humans, and bone, lymphoid, salivary and thyroid cancers in rodents.

Establishment of the estradiol ADI is in sharp variance with evidence on the extreme sensitivity of infants and pre-pubertal children to hormonal carcinogens. Furthermore, a growing literature on "hormonal imprinting" strongly suggests that exogenous hormonal influences in infancy and critical phases of sexual maturation determine hormonal responsiveness and carcinogenic risks in adult life.

Establishment of the 1999 ADI ignores evidence on additive and/or synergistic interactions between estradiol and other simultaneously implanted hormones. Illustrative are the synergistic effects of estradiol and progesterone in the induction of mammary tumors in mice and prostate cancer in rats. Failure to address these concerns also contrasts with 1997 testimony by a lead US/Canadian expert that "— studies relating to the genotoxicity or carcinogenicity of hormone combinations have not been carried out even though this is frequently the preferred method of use"; establishment of the ADI also ignores synergistic interactions between estrogens and other unrelated carcinogens.

JECFA 1999 admits that estradiol, besides progesterone and testosterone, residues are "statistically significantly higher than in corresponding values in concurrent controls." Nevertheless, JECFA concludes that monitoring for such excess residues is unnecessary.

JECFA appears unaware that ultrasensitive hormonal assays in pre-pubertal children, as reported in 1994, have shown that daily production rates of estradiol may have been over estimated by 100-fold. Thus, residues in organs/tissues of implanted cattle could be well in excess of ADI levels.

JECFA appears unaware of serious concerns on environmental contamination, particularly of drinking water, from fecal and urinary excretion of hormones by millions of cattle continuously processed through feed lots. Of equal concern is the reported sale to rendering plants of discarded ears of slaughtered cattle containing very high levels of residual hormones for potential uses including animal feed, pet food, and manufacture of gelatin and glycerol for cosmetics, foods and pharmaceutical products.

Finally, serious concerns persist with regard to the selection procedures, composition, scientific competence and conflicts of interest in JECFA, apart from their reliance on unpublished industry data and lack of procedural transparency.